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combined inhibition of ALK5 and CTGF (show CTGF Proteins) is required to prevent TGFbeta (show TGFB1 Proteins)-induced nodule formation in tri (show VANGL2 Proteins)-cellular cultures
Aortic diseases in patients with TGFBR1 or TGFBR2 (show TGFBR2 Proteins) mutations show the same prevalence of systemic features and the same global survival.
Results show that TGFBR1 expression is regulated in bladder cancer cell through its desumoylation by SENP2.
Low TGFBR1 expression is associated with oral cancer progression.
TGF-beta (show TGFB1 Proteins) type I, II, and III receptors were all identified in pregnant serum; all were substantially elevated in early-onset but not late-onset preeclampsia. Endoglin (show ENG Proteins) was increased in both subtypes.
Overexpression of truncated ALK5 in a B-cell line counteracted BMP-7 (show BMP7 Proteins)-induced apoptosis, whereas overexpression of truncated ALK4 (show ACVR1B Proteins) had no effect.
Although TGFbeta1 (show TGFB1 Proteins)/2 receptors are downregulated in breast cancer, their expression in tumors is an indicator of aggressive breast cancer phenotype.
Higher proportions of early-onset Diffuse Gastric Cancers (DGCs) contained somatic mutations in CDH1 (show CDH1 Proteins) or TGFBR1 compared with late-onset DGCs. A smaller proportion of early-onset DGCs contained somatic mutations in RHOA (show RHOA Proteins). CDH1 (show CDH1 Proteins) alterations, but not RHOA (show RHOA Proteins) mutations, were associated with shorter survival times. Female predominance in early-onset DGC (show GGCX Proteins) may be related to relatively high rates of somatic CDH1 (show CDH1 Proteins) and TGFBR1 mutations.
Coronin 1B (show CORO1B Proteins) constitutively binds to TGF beta (show TGFB1 Proteins) receptor I in vascular smooth muscle cells.
BIX02189 is a potent inhibitor of TGF-beta type I receptor that can block the lung tumor metastatic activity of TGF-beta1 (show TGFB1 Proteins).
The results indicate that the TGFBR1 gene polymorphism (SNP64) is significantly associated with growth rates including average daily gains between birth and 56 kg, between 5.5 and 56 kg, between 35 and 56 kg.
Report temporal regulation of TGFBR1 mRNA expression in the oocyte, granulosa and theca cells of developing preovulatory follicles in the pig.
TGFbeta (show TGFB1 Proteins) is abundant in boar seminal plasma, thus TGFbeta (show TGFB1 Proteins) may be a male-female signalling agent involved in immune changes in the female reproductive tract elicited by seminal fluid.
Porcine transforming growth factor beta receptor 1 has many polymorphisms, including two nonsynonymous substitutions in exons 1 and 7 and novel alternative splicing in exon 3.
isolation and molecular characterization; the full-length TGFBR1 cDNA 1813 bp contains an open reading frame (ORF) of 1512 bp encoding a TGFBR1 protein of 503 amino acids with a calculated molecular weight of 56.4 kDa.
Results show that ALK5 and ALK1 (show ACVRL1 Proteins) play antagonistic roles in TGF-beta (show TGFB1 Proteins)-induced podosome formation in aortic endothelial cells.
This study showed that ubiquitinated ALK5 and phosphorylated heat shock protein 27 specifically accumulate in the cytoskeleton fraction, and ALK1 (show ACVRL1 Proteins) and ALK5 interact with heat shock protein 90 (show HSP90 Proteins).
GM-CSF (show CSF2 Proteins) induced airway smooth muscle cells to increase expression of transforming growth factor (TGF)-beta (show TGFB1 Proteins) receptors type I, II, and III, but had no detectable effect on the release of TGF-beta1 (show TGFB1 Proteins) by the same ASMC; corticosteroids were inhibitory
ALK5 and Smad4 (show SMAD4 Proteins) have roles in TGF-beta1 (show TGFB1 Proteins)-induced pulmonary endothelial permeability
These results indicate that high plasma cholesterol levels may contribute to the pathogenesis of certain diseases (e.g., atherosclerosis) by suppressing TGF-beta (show TGFB1 Proteins) responsiveness.
Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5.
ALK1 and ALK5 are both essential for correct regulation of VEGF, and that disruption of either pathway leads to disease.
TGF-beta1 (show TGFB1 Proteins) downregulates caveolin-1 (show CAV1 Proteins) of cultured endothelial cells, involving ALK-5 receptor subtype
Conditional deletion of Tgfbr1 in PTEN-inactivated endometrium leads to a disease that recapitulates invasive and lethal human endometrial cancer.
fluid shear stress induces autocrine TGF-beta (show TGFB1 Proteins)/ALK5-induced target gene expression in renal epithelial cells, which is partially restrained by MEK1 (show MAP2K1 Proteins)/2-mediated signaling.
both GDF-15 (show GDF15 Proteins) and TGF-beta1 (show TGFB1 Proteins) counteract chemokine (show CCL1 Proteins)-induced integrin activation on neutrophils via the ALK-5/TGF-betaRII heterodimer.
CD109 (show CD109 Proteins) differentially regulates TGF-beta (show TGFB1 Proteins)-induced ALK1 (show ACVRL1 Proteins)-Smad1 (show SMAD1 Proteins)/5 versus ALK5-Smad2 (show SMAD2 Proteins)/3 pathways, leading to decreased extracellular matrix production in the skin; epidermal CD109 (show CD109 Proteins) expression regulates dermal function through a paracrine mechanism
miR (show MLXIP Proteins)-27b is an anti-fibrotic microRNA that inhibits fibroblast activation by targeting TGFbeta (show TGFB1 Proteins) receptor 1 and SMAD2 (show SMAD2 Proteins).
In the presence of gadolinium and antibeta1 integrin antibody, collagen regulated the expression levels of Tgfbr1, Tgfbr2 (show TGFBR2 Proteins) and Smad2 (show SMAD2 Proteins)/3, but did not alter the phosphorylation of p38 (show CRK Proteins), ERK1/2 or JNK (show MAPK8 Proteins).
miR (show MLXIP Proteins)-22 acts as a novel negative regulator of angiotensin II-induced cardiac fibrosis by suppressing the expression of TGFbetaRI in the heart.
TGFbetaRI inhibition in an injured adult heart could both stimulate the autocrine/paracrine activity of survivin (show BIRC5 Proteins) and inhibit Wnt (show WNT2 Proteins) in CPCs to mediate cardioprotection and improve cardiac function.
Data show that transforming growth factor-beta receptor I (Tgfbr1) was a direct target of microRNA miR (show MLXIP Proteins)-140-5p.
Targeted early inactivation of Alk5 in mesodermal progenitors caused abnormal development and maturation of the lung that included reduced physical size of the sub-mesothelial mesoderm, an established source of specific mesodermal progenitors.
The protein encoded by this gene forms a heteromeric complex with type II TGF-beta receptors when bound to TGF-beta, transducing the TGF-beta signal from the cell surface to the cytoplasm. The encoded protein is a serine/threonine protein kinase. Mutations in this gene have been associated with Loeys-Dietz aortic aneurysm syndrome (LDAS). Multiple transcript variants encoding different isoforms have been found for this gene.
TGF-beta receptor type I
, TGF-beta receptor type-1
, TGF-beta type I receptor
, activin A receptor type II-like kinase, 53kD
, activin A receptor type II-like kinase, 53kDa
, activin A receptor type II-like protein kinase of 53kD
, activin receptor-like kinase 5
, serine/threonine-protein kinase receptor R4
, transforming growth factor beta receptor I
, transforming growth factor, beta receptor I (activin A receptor type II-like kinase, 53kD)
, transforming growth factor-beta receptor type I
, transforming growth factor, beta receptor 1 (activin A receptor type II-like kinase, 53kDa)
, transforming growth factor, beta receptor I (activin A receptor type II-like kinase, 53kDa)
, transforming growth factor beta type I receptor
, transforming growth factor, beta receptor 1
, transforming growth factor beta receptor 1
, activin A receptor type II-like kinase
, transforming growth factor beta receptor type I
, transforming growth factor beta, receptor 1
, type I serine/threonine kinase receptor
, TGF-beta receptor type-1-like
, transforming growth factor, beta receptor I